title: Susceptibility to upper airway obstruction during partial neuromuscular block.
abstract: BACKGROUND
  Airway obstruction after anesthesia may be caused or exaggerated by residual neuromuscular block, with loss of muscle support for collapsible upper airway structures.
  
  
  METHODS
  Six male volunteers were studied before treatment, during stable partial neuromuscular block with vecuronium at a mean train-of-four (TOF) ratio of 50% (95% CI, 36-61%), and after reversal by neostigmine. Catheter-mounted transducers were placed in the pharynx and esophagus to estimate, respectively, the upper airway resistance, and the work of breathing (calculated as the time integral of the inspiratory pressure developed by the respiratory muscles, esophageal pressure time product) during quiet breathing, during breathing 5% carbon dioxide, and while breathing with an inspiratory resistor. Breathing with pressure at the airway opening held at pressures from -5 to 40 cm H2O were also tested to assess airway collapsibility.
  
  
  RESULTS
  Although breathing through a resistor increased upper airway resistance from 1.2 (0.67, 1.72) cm H2O x l(-1) x s to 2.5 (1.32, 3.38) cm H2O x l(-1) x s, and carbon dioxide stimulation reduced resistance to 0.8 (0.46, 1.33) cm H2O x l(-1) x s, no effect of partial neuromuscular block (mean TOF ratio, 52%) on upper airway properties could be shown.
  
  
  CONCLUSIONS
  Neuromuscular block with a TOF ratio of 50% can be present yet clinically difficult to detect in patients recovering from anesthesia. This degree of block has no effect on airway patency in volunteers, even during challenge. Airway obstruction during recovery from anesthesia thus is more likely to be caused by residual effects of general anesthetic agents or centrally acting analgesics, either alone or perhaps in concert with residual neuromuscular block.
authors.affiliation: University of Paris XII, Hôpital Henri Mondor, Créteil, France.
authors.forename: G
authors.initials: G
authors.lastname: D'Honneur
authors.forename: F
authors.initials: F
authors.lastname: Lofaso
authors.forename: G B
authors.initials: GB
authors.lastname: Drummond
authors.forename: J M
authors.initials: JM
authors.lastname: Rimaniol
authors.forename: J V
authors.initials: JV
authors.lastname: Aubineau
authors.forename: A
authors.initials: A
authors.lastname: Harf
authors.forename: P
authors.initials: P
authors.lastname: Duvaldestin
mesh_terms: D000328:Adult; D000402:Airway Obstruction / Q000139:chemically induced*; D000403:Airway Resistance / Q000187:drug effects; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D004198:Disease Susceptibility; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D009388:Neostigmine / Q000494:pharmacology; D019148:Neuromuscular Blockade; D003473:Neuromuscular Nondepolarizing Agents / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D014673:Vecuronium Bromide / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D014939:Work of Breathing / Q000187:drug effects
chemical_list: D002800:Cholinesterase Inhibitors; D003473:Neuromuscular Nondepolarizing Agents; D009388:Neostigmine; D014673:Vecuronium Bromide